Atherosclerotic cardiovascular disease is a common cause of death in industrialized countries (AJR 150:1263-1269 (1988)), and is characterized by a narrowing of the arterial lining due to atherosclerotic plaques. Surgical methods of treating this disease, including bypass techniques, have resulted in significant medical advancement. A need exists however, for a treatment with less expensive and less invasive procedures.
Percutaneous transluminal angioplasty, or balloon angioplasty, of peripheral and coronary arteries has proven to be a useful nonsurgical procedure for the treatment of localized arterial lesions due to atherosclerosis, and has become a promising non-surgical alternative to bypass surgery. (Merck Manual, 15th Ed. p. 559). The technique consists of inserting an uninflated balloon-tipped catheter into the affected artery. Dilation of the diseased segment of artery is accomplished by inflating the balloon which pushes the atherosclerotic lesion outward, thereby enlarging the arterial diameter. Typically, inflation is repeated two additional times. The balloon is then deflated and the catheter is withdrawn.
Following balloon angioplasty, blood flow through the artery is usually significantly improved. The primary success rate of the technique is around 90-95%. Intimal flap, abrupt occlusion due to acute thrombus formation, dissection of the artery, elastic recoil of the vessel wall, and the inability to pass the stenotic area however, are mostly responsible for acute failure of the procedure. In addition, long term success is complicated by a high rate (35-40%) of late restenosis usually within 3 to 6 months. As a result, about one-third of all patients treated with balloon angioplasty return for a second or third procedure. (Eur. Heart J. 9:31-37 (1988)). A need exists therefore, for a method to decrease acute failure and increase the long-term benefits of balloon angioplasty, with the aim of preventing restenosis of the diseased vessel.
The physiological basis of restenosis after balloon angioplasty is an accelerated, probably modified smooth muscle cell proliferation and secondary ground substance (collagen, etc.) deposition initiated by the angioplasty procedure itself. This accelerated proliferation of cells primarily results from the extensive traumatic damage to the vessel wall which occurs following conventional balloon dilation, partially due to the pressures (6-12 atm) applied to overcome the elastic recoil. The traumatic damage includes stretching of the media and adventitia. This leads in turn to growth factor expression in the smooth muscle and adventitial cells which stimulates cell proliferation and an "overshot" of the normal healing process, as in keloid formation. In addition, irregular intimal tears occur which expose the deeper highly thrombogenic layers of the vessel to the blood and provoke attachment of cellular elements such as platelets, neutrophils and monocytes, with deliberation of growth factors such as platelet derived growth factor (PDGF). (Walker et al, Proc. Acad. Sci 83:7311-7315 (1986)). Further, it has recently been suggested that the mechanism of balloon dilation primarily affects the normal vessel wall (vs. the diseased areas), inducing a higher proliferative response from the normal area. (Gravanis et al, Human Pathol 20:477-485 (1989)).
Other techniques to recanalize diseased vessels or make incisions in a vessel wall have been described, but those that remove the bulk of the atherosclerotic lesion actually provoke more extended injury in the vessel and result in a higher reparative/proliferative response than with balloon angioplasty. (Simpson et al, Circ. 90(4):2311A (1989)). Ginsburg et al., U.S. Pat. No. 4,790,310 combines laser and balloon angioplasty to reopen stenosed arteries; Bonnet, U.S. Pat. No. 4,712,547 describes an instrument for slitting stenosis in the ureter; Korth, et al., U.S. Pat. No. 4,633,860 relates to a device that creates incisions in the skin and tissue beneath the skin, forming a canal for inserting an endoscope for percutaneous nephroscopy; Lary, U.S. Pat. No. 4,273,128 describes a surgical instrument for coronary cutting and dialating a vessel or to "valve" a stenotic mass to facilitate smooth introduction of a balloon catheter to the center of the stenosis; Hoffman, U.S. Pat. No. 2,730,101 describes a cutter means usable clogged milk ducts; Richter, U.S. Pat. No. 2,655,154 describes a valvulotome for operating on the pulmonary valve; Hallman, U.S. Pat. No. 518,600 describes an instrument for cutting urethral strictures; and USSR publication 938977 depicts a retractable blade extendable by pneumatic pressure. None of these devices and methods is intended for increasing the diameter of a vessel by producing regular longitudinal surgical cuts in the vessel wall, and decreasing or eliminating subsequent secondary cellular proliferation or restenosis. Many of these devices may actually provoke a higher reparative/proliferative response.